Don't understand H Pylori pathogenesis

[yoyohomieg5432]

Can anyone explain to me what H pylori is doing? First aid says that chronic gastritis with pylori is causes hypochlorhydria and hypergastrinemia. If this is the case, why do people get ulcers if the acid levels are low?

UW is saying contradictory, that pylori increases gastric acid secretion (#7710). So I really have no idea what pylori is actually doing.

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[DerpStore]

I've been a little confused by this too but haven't taken the time to really get to the bottom of it... this article below made a lot of sense though. From skimming through uptodate the pathogenesis seems to be quite complicated but I think the following is an adequate summary.

When h. pylori infection is limited to the antral region, the acid secreting region of stomach is relatively spared. H. pylori can inhibit D cells from producing somatostatin, which will lead to an increase in gastrin and subsequently acid production which will lead to duodenal ulceration.

When the infection affects the whole stomach (pangastritis) acid production will be decreased. The gastric ulcerations here will be secondary to the inflammatory response, not acidification.

http://www.pathologystudent.com/?p=2169

 

[Transposony]

 

[soop]

H. pylori infection results in two broad types of infection. They can be classified as antrum infections vs fundus infections. Both are considered chronic gastritis. Both can cause ulcers, though the location of ulcers are typically different.

Antrum infection: Urease splits urea & the resulting ammonium → destroys the mucous barrier. → inflammatory damage to gastric D-cell damage → ↓ somatostatin secretion → hypersecretion of gastric acid → duodenal ulcers that are usually in the bulb. There is no increased risk of gastric adenocarcinoma with this type of gastritis.

Fundus infections: Similar to autoimmune gastritis in the sense that it's an atrophic type of gastritis. Damage to the parietal cells → ↓ HCl secretion → ↑ gastrin secretion. However, the concomitant inflammation → ↓ PG secretion → ↓ mucoprotective barrier → mucosa damage even with the low levels of gastric HCl → progression to gastric ulcers. This type of infection does increase the risk of gastric adenocarcinoma (intestinal type only) as well as MALTomas.